Changes

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| Also known as:

| Also known as:

| '''Theiler's disease<br>

| '''Theiler's disease<br>Equine Serum Hepatitis<br>ESH

|}

|}

The affected animal's history often includes administration of an equine-derived biologic product approximately four to six weeks prior to the onset of clinical signs. Clinical signs are generally sudden in onset and rapidly progressive.  

The affected animal's history often includes administration of an equine-derived biologic product approximately four to six weeks prior to the onset of clinical signs. Clinical signs are generally sudden in onset and rapidly progressive.  

Signs may range from mild non-specific signs of lethargy, weight loss or inappetance to signs of acute or chronic hepatic failure. Affected horses are often severely icteric and pass dark urine due to the presence of bilirubin. Signs relating to hepatic encephalopathy may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as photosensitisation or pruritus may also be seen. The course of the disease is usually around five days, with death ususally occuring within ten days.  

Signs may range from mild non-specific signs of lethargy, weight loss or inappetance to signs of acute or chronic hepatic failure. Affected horses are often severely icteric and pass dark urine due to the presence of bilirubin. Signs relating to [[Hepatic Encephalopathy - Horse|hepatic encephalopathy]] may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as [[Photosensitisation|photosensitisation]] or pruritus may also be seen. The course of the disease is usually around five days, with death usually occurring within ten days.  

Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.  

Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.  

==Diagnosis==

==Diagnosis==

Diagnosis of ESH and evaluation of hepatic function may be achieved using a combination of clinical history, abrupt onset of clinical signs and diagnostic tests indicative of hepatic insufficiency. Serum biochemistry may indicate the following abnormalities:

Diagnosis of ESH and evaluation of hepatic function may be achieved using a combination of clinical history, abrupt onset of clinical signs and diagnostic tests indicative of hepatic insufficiency.  

 

* Increased conjugated and unconjugated bilirubin

* Increased conjugated and unconjugated bilirubin

* Increased liver enzymes- SDH, AST, GGT and ALP

* Increased liver enzymes- SDH, AST, GGT and ALP

* Increased urea

* Increased urea

 

'''Ultrasound''' may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts. In several studies, biopsy is considered as the ‘gold standard’ technique for definitive diagnosis of hepatic disease. Biopsy is usually performed on the right hand side between the twelth and fourteenth intercostal spaces. A coagulation profile is often performed prior to performing the procedure due to the possibility of a clotting defect.  

Ultrasound may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts. In several studies, biopsy is considered as the ‘gold standard’ technique for definitive diagnosis of hepatic disease. Biopsy is usually performed on the right hand side between the twelth and fourteenth intercostal spaces. A coagulation profile is often performed prior to performing the procedure due to the possibility of a clotting defect.  

==Pathology==

==Pathology==

Post mortem examination often shows generalised icterus and ascites, with an enlarged and pale liver. Histologically there may be signs of acute hepatocellular degeneration including centrilobular to midzonal necrosis, with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.  

''Post mortem'' examination often shows generalised [[Icterus|icterus]] and ascites, with an enlarged and pale liver. Histologically there may be signs of acute hepatocellular degeneration including centrilobular to midzonal necrosis, with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.  

==Treatment==

==Treatment==

The aims of treatment are mainly to support liver function until hepatic compromise can occur. Affected horses should be housed in a quiet, darkened stable in order to minimise stimulation. Sedation may be required if signs of hepatic encephalopathy are present. Stressful situations such as moving the horse or separation from field mates should be avoided.

The aims of treatment are mainly to support liver function until hepatic compromise can occur. Affected horses should be housed in a quiet, darkened stable in order to minimise stimulation. Sedation may be required if signs of hepatic encephalopathy are present. Stressful situations such as moving the horse or separation from field mates should be avoided.

If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. In order to reduce the severity of neurological signs, the protein should be high in branched-chain amino acids; corn and molasses are often used to achieve this. If the horse is anorexic, a naso-gastric tube can be passed and high energy foods given directly into the stomach.

 

If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. In order to reduce the severity of neurological signs, the protein should be high in branched-chain amino acids; corn and molasses are often used to achieve this. If the horse is anorexic, a [[Nasogastric intubation of the horse|naso-gastric tube]] can be passed and high energy foods given directly into the stomach.

==Prognosis==

==Prognosis==

[[Category:To_Do_-_SophieIgnarski]]

[[Category:To_Do_-_SophieIgnarski]]